[Autoimmune reactions against interleukin-2 receptors in patients with blood system diseases and in experimental Rauscher retrovirus leukemia]. / Autoimmunnye reaktsii protiv retseptorov dlia interleikina-2 u bol'nykh s nekotorymi zabolevaniiami sistemy krovi i pri éksperimental'nom retrovirusnom leikoze Raushera.

Apart from autoimmune reactions, antibodies to IL-2 receptors were identified in blood sera of linear mice during leukemogenesis. It is indicated that in the course of leukemia establishment, there can be demonstrated antibodies capable of blocking IL-2 receptors on the membrane of activated T lymphocytes and inhibiting IL-2-dependent proliferation of T cells. The blood sera of patients suffering from chronic lymphoid leukemia, acute lymphoblastic leukemia, lymphocytomas, pure red-cell aplasia, and aplastic anemia showed antibodies against IL-2 receptors. Out of the total number of 52 patients, 23 demonstrated those antibodies. The data obtained should be taken into account in the patients' management using IL-2.

[Humoral autoimmune reactions directed against autoantigens of the H-2 histocompatibility system in mice with developing Rauscher leukemia]. / Gumoral'nye autoimmunnye reaktsii myshei s razvivaiushchimsia leikozom Raushera, napravlennye protiv sobstvennykh antigenov gistosovmestimosti sistemy H-2.

Antibodies exhibiting a selective anti-H-2 haplotype reaction with thymic and splenic lymphocytes of intact mice were found in the sera of mice of the strains BALB/c, C57Bl/6, AKR and BDF1 with the developing Rauscher leukemia by applying the membrane immunofluorescent and complement-dependent cytotoxicity techniques in vitro. Monoclonal antibodies against H-2 IAd and H-2 IAk and sorption tests using lymphocytes of the congenic-resistant strains as target cells were used to show that the aforementioned antibodies acted against autoantigens which are the products of the genes of the I-subregion of the H-2 histocompatibility complex.

[Antilymphocytic humoral autoimmune response of mice with developing Rauscher leukemia directed against group-specific retrovirus antigens]. / Antilimfotsitarnye gumoral'nye autoimmunnye reaktsii myshei s razvivaiushchimsia leikozom Raushera, napravlennye protiv gruppospetsificheskikh antigenov retrovirusov.

The methods of indirect membrane immunofluorescence, immunoenzyme analysis, complement-dependent cytotoxicity and sorption tests were used to demonstrate two types of humoral antilymphocytic autoimmune reactions at the early stage of the Rauscher leukemia in mice of BALB/c, BDF1 and C57B1/6 strains. The first one is directed against group-specific oncoviral antigens (p30, p15) expressed on the lymphocyte membrane of both intact mice and of those with leukemia, the second one is virus-independent and possesses strain specificity.

[Autogenic anti-idiotypic suppression of autoimmune reactions--a new approach to immunotherapy of experimental leukemia]. / Autogennoe antiidiotipicheskoe podavlenie autoimmunnykh reaktsii--novyi podkhod k immunoterapii eksperimental'nykh leikozov.

Experimental Rauscher's virus erythroleukemia (RVE) was employed to study the immunologic mechanisms by which leukemia develops. Experiments were performed on inbred mice, genetically opposite to the disease induction, namely on highly sensitive BALB/c, resistant C57BL/6 and moderately sensitive BDFI animals. It is shown that RVE resistance is an immunologic phenomenon that results from the functioning of the antileukemic immune defence (ALID) aimed against the tumor-specific antigenic complex. Suppression of the ALID stems from autosuppression of the H-2 complex of the histocompatibility antigen system of T suppressors, which leads to the development of the onco-specific complex of autoimmune responses (OSCAR) and to the obligate development of RVE. The recovery of the ALID with OSCAR suppression and RVE regression is a consequence of the development of strictly specific antiidiotypic immune responses (antibodies AIT-anti-OSCAR). It is demonstrated that both passive administration of AIT-anti-OSCAR and induction of their active synthesis brings about a remission of RVE.